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#28945763   2017/09/25 Save this To Up

Toxicological effects of NCKU-21, a phenanthrene derivative, on cell growth and migration of A549 and CL1-5 human lung adenocarcinoma cells.

Chemotherapy insensitivity continues to pose significant challenges for treating non-small cell lung cancer (NSCLC). The purposes of this study were to investigate whether 3,6-dimethoxy-1,4,5,8-phenanthrenetetraone (NCKU-21) has potential activity to induce effective toxicological effects in different ethnic NSCLC cell lines, A549 and CL1-5 cells, and to examine its anticancer mechanisms.

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Epidermal Growth Factor ( Epidermal Growth Factor ( Rabbit Anti-Human Red Blo Anti C Reactive Protein A Epidermal Growth Factor ( Epidermal Growth Factor ( Fibroblast Growth Factor Fibroblast Growth Factor Fibroblast Growth Factor Fibroblast Growth Factor Keratinocyte Growth Facto Keratinocyte Growth Facto

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#28393656   2017/04/10 Save this To Up

Punicalagin reduces H2O2-induced cytotoxicity and apoptosis in PC12 cells by modulating the levels of reactive oxygen species.

Oxidative stress has long been linked to neuronal cell death in many neurodegenerative diseases. Antioxidant conventional supplements are poorly effective in preventing neuronal damage caused by oxidative stress due to their inability to cross the blood brain barrier. Hence the use of molecules extracted from plants and fruits such as phenolics, flavonoids, and terpenoids compounds constitute a new wave of antioxidant therapies to defend against free radicals.

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#28147711   2017/02/02 Save this To Up

Pharmacokinetics and in vitro and in vivo delivery of sulforaphane by PCL-PEG-PCL copolymeric-based micelles.

A reliable and efficient drug delivery system using PCL-PEG-PCL copolymers was established for the anti-cancer compound sulforaphane (SF) in this study. Encapsulated SF by PCL-PEG-PCL nanoparticles led to formation of SF-loaded PCL-PEG-PCL micelles. Micelles characterization and stability, the particle size and their morphology were determined by DLS and AFM. The loading efficiency of SF was 19.33 ± 1.28%. The results of AFM showed that the micelles had spherical shapes with the size of 107 nm. In vitro release of SF from SF-entrapped micelles was remarkably sustained. The cytotoxicity of free SF, PCL-PEG-PCL and SF/PCL-PEG-PCL micelles was analysis by MTT colorimetric assay on MCF-7, 4T1 and MCF10A cell lines. Expression levels of BCL-2, PARP, COX-2, Caspase-9 and ACTB genes were quantified by real-time PCR. Flow cytometry analysis was performed using the Annexin V-FITC Apoptosis Detection Kit to evaluate the apoptotic effects of free SF compared with SF/PCL-PEG-PCL micelles. Study of the in vivo pharmacokinetics of the SF-loaded micelles was carried out on SF-loaded PCL-PEG-PCL micelles in comparison with free SF. The results of in vivo experiments indicated that the SF loaded micelles significantly reduced the tumor size. In vivo results showed that the multiple injections of SF-loaded micelles could prolong the circulation period and increase the therapeutic efficacy of SF. Also, in comparison with the free-SF solution, encapsulation of the SF in micelles increased the mean residence time from 0.5 to 4 h and the area under the concentration-time curve up to 50 folds.

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C Peptide ELISA Kit, Rat Directed In Vivo Angiogen Cultrex In Vitro Angiogen Human integrin aVb3, affi BYL-719 Mechanisms: PI3K- Inhibitory Mouse Monoclon Inhibitory Mouse Monoclon MarkerGeneTM in vivo lacZ Resorufin Oleate, Fluorog Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti Sterile filtered goat se

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#27899859   2016/11/30 Save this To Up

Effect of N-Perfluorooctane on Hypoxia/Reoxygenation Injury in Human Umbilical Vein Endothelial Cells.

This study investigated the effect of n-perfluorooctane (PFC) on hypoxia/reoxygenation (H/R) injury in human umbilical vein endothelial cells (HUVECs).

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Human Umbilical Vein Endo GFP Expressing Human Umbi Mitochondria GFP Tag Huma Plasma Membrane GFP Tag H RFP Expressing Human Umbi Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Human Saphenous Vein Endo GFP Expressing Human Saph RFP Expressing Human Saph

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#27525394   2016/08/16 Save this To Up

[Investigation of antitumorigenic effects of food-borne non-pathogenic and pathogenic Salmonella enterica strains on MEF, DU145 and HeLa cell lines].

Basic applications in cancer therapy may fail to eradicate cancer cells completely, they can show toxic affects to healthy cells and development of resistance to antitumor agents may increase tendency to metastasis. Bacterial therapies have the advantage of specific targetting of tumors by selective toxicity, responsiveness to external signals, self-propelling capacity, and the sense of microenvironment. The most interest on the bacterial cancer therapy is about Salmonella spp. with a special emphasis of S.Typhimurium. The aim of this study was to investigate the antitumorigenic effects of food-borne non-pathogenic and pathogenic Salmonella enterica strains on different cell cultures. Non-pathogenic Salmonella Enteriditis (A17) and pathogenic Salmonella Telaviv (A22) strains isolated from chicken carcasses which were put on the market in Edirne province (located at Thrace region of Turkey), and Salmonella Typhimurium ATCC 14028 strain were used in the study. ATCC-derived MEF (mouse embryonic fibroblasts), DU145 (human prostate cancer cells), and HeLa (human cervical cancer cells) cell lines were cocultivated with Salmonella strains of MOI (Multiplicity of infection; number of bacteria:number of cell) of 1000:1, 100:1, 10:1, 1:1, 0.1:1. The cell viability was measured by colorimetric MTT cytotoxicity assay, the percentage of apoptosis was assessed by Tali® Apoptosis Assay-Annexin V Alexa Fluor® 488 kit (Invitrogen, Molecular Probes, Life Technologies, USA), and the caspase-3 activity was determined by colorimetric protease ApoTarget™ kit (Invitrogen, BioSource International, USA). It was shown that non-pathogenic S.Enteriditis (A17) decreased cell viability approximately to 70%, wheras patogenic S.Telaviv (A22) and standart S.Typhimurium ATCC 14028 strains reduced cell viability approximately to 80%. Adversely, it was also observed that pathogenic S.Telaviv (A22) strain induces apoptosis more effectively than non-pathogenic S.Enteriditis (A17) and S.Typhimurium ATCC 14028 strains. Apoptosis percentage induced by pathogenic S.Telaviv (A22) strain was approximately 15% while 5% for both non-pathogenic S.Enteriditis (A17) and S.Typhimurium ATCC 14028 strains. Similarly, average OD405 values of caspase-3 activity was shown as 0.01 for both non-pathogenic S.Enteriditis (A17) and S.Typhimurium ATCC 14028 strains whereas average OD405 value of caspase-3 activity for pathogenic S.Telaviv (A22) strain was very close to 0.02 and it doubled the value for negative control. Our data are important in terms of the indication of food-borne pathogenic S.Telaviv (A22) strain that enhanced caspase-3 activity and induced apoptosis, and S.Enteriditis (A17) strain that showed selective cytotoxicity on DU145 (human prostate cancer cells).

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Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 GLP 2 ELISA Kit, Rat Prog Screen Quest™ Fluo 8 Me Screen Quest™ Fluo 8 Me Cal-520™ Medium Removal Cal-520™ Medium Removal Cal-520™ No-Wash Calciu Cal-520™ No-Wash Calciu

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#27469140   2016/09/01 Save this To Up

Isoflurane Preconditioning Induces Neuroprotection by Up-Regulation of TREK1 in a Rat Model of Spinal Cord Ischemic Injury.

This study aimed to explore the neuroprotection and mechanism of isoflurane on rats with spinal cord ischemic injury. Total 40 adult male Sprague-Dawley rats were divided into the four groups (n=10). Group A was sham-operation group; group B was ischemia group; group C was isoflurane preconditioning group; group D was isoflurane preconditioning followed by ischemia treatment group. Then the expressions of TWIK-related K⁺ channel 1 (TREK1) in the four groups were detected by immunofluorescent assay, real time-polymerase chain reactions (RT-PCR) and western blot. The primary neurons of rats were isolated and cultured under normal and hypoxic conditions. Besides, the neurons under two conditions were transfected with green fluorescent protein (GFP)-TREK1 and lentivirual to overexpress and silence TREK1. Additionally, the neurons were treated with isoflurane or not. Then caspase-3 activity and cell cycle of neurons under normal and hypoxic conditions were detected. Furthermore, nicotinamide adenine dinucleotide hydrate (NADH) was detected using NAD+/NADH quantification colorimetric kit. Results showed that the mRNA and protein expressions of TREK1 increased significantly in group C and D. In neurons, when TREK1 silenced, isoflurane treatment improved the caspase-3 activity. In hypoxic condition, the caspase-3 activity and sub-G1 cell percentage significantly increased, however, when TREK1 overexpressed the caspase-3 activity and sub-G1 cell percentage decreased significantly. Furthermore, both isoflurane treatment and overexpression of TREK1 significantly decreased NADH. In conclusion, isoflurane-induced neuroprotection in spinal cord ischemic injury may be associated with the up-regulation of TREK1.

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DNA (cytosine 5) methyltr Goat Anti-Rat MARCH10, (i Goat Anti-Mouse, Rat DLL1 Goat Anti-Human, Mouse, R Goat Anti-Human, Mouse, R Goat Anti-Rat Connexin 43 Goat Anti-Human, Rat CHRN Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki

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#27446455   2016/07/22 Save this To Up

Paeoniflorin inhibits human pancreatic cancer cell apoptosis via suppression of MMP-9 and ERK signaling.

Paeoniflorin exhibits anticancer, anti-inflammatory and antioxidation effects, as well as specific pharmacological effects on smooth muscle and the immune, cardiovascular and central nervous systems. The present study aimed to investigate the anticancer effects of paeoniflorin on pancreatic cancer cells and to elucidate the mechanisms by which these effects occur. In the present study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assays were performed to assess cell viability and cell cytotoxicity of BXPC-3 human pancreatic cancer cells, respectively. Cellular apoptosis and caspase-3/9 activities were analyzed using an Annexin V-fluorescein isothiocyanate/propidium iodide Apoptosis Detection kit, a DAPI staining assay and colorimetric kits, respectively. Matrix metalloproteinase-9 (MMP-9) and extracellular signal-regulated kinases (ERK) protein expression in BXPC-3 cells were also investigated using gelatin zymography assays and western blot analysis, respectively. In the present study, paeoniflorin was found to inhibit the cell viability and increase cell cytotoxicity of BXPC-3 cells in a dose- and time-dependent manner. In addition, cellular apoptosis, as well as caspase-3 and -9 activity of BXPC-3 cells was increased following paeoniflorin treatment. Notably, paeoniflorin reduced MMP-9 and ERK protein expression in BXPC-3 cells. These results indicate that paeoniflorin exhibits a potential anticancer effect by enhancing human pancreatic cancer cell apoptosis via the suppression of MMP-9 and ERK signaling.

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anti Transferrin receptor Human Mouse Rat Phospho-E Human Mouse Rat Phospho-E anti H inh human blood an Glucagon ELISA KIT, Rat G anti CD7 All T cells Reco Human T Cell Receptor Sig Human Pancreatic Microvas Human Phospho-EGFR (Activ Human Mouse Rat Phospho-E Human Phospho-EGFR (Y1068 Human Mouse Rat Phospho-E

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#27446379   2016/07/22 Save this To Up

Psoralidin inhibits proliferation and enhances apoptosis of human esophageal carcinoma cells via NF-κB and PI3K/Akt signaling pathways.

Esophageal cancer is the most common gastrointestinal cancer. Psoralidin exhibits antioxidant, anti-apoptotic, anti-inflammatory and antitumor effects, which result in the inhibition of cancer formation. The present study aimed to investigate the effect of psoralidin on esophageal carcinoma proliferation and growth, and to elucidate its underlying mechanism of action. The effect of psoralidin on cell proliferation was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Using an annexin V-fluorescein isothiocyanate/propidium iodide apoptosis detection kit and 4',6-diamidino-2-phenylindole staining assay, the present study demonstrated that psoralidin significantly enhanced apoptosis of human esophageal carcinoma Eca9706 cells. In addition, caspase-3 activity was analyzed with a caspase-3 colorimetric assay kit, while nuclear factor (NF)-κB activity and protein phosphatidylinositol 3-kinase (PI3K)/Akt expression were measured with an NF-κB enzyme-linked immunosorbent assay kit and western blot analysis, respectively. Eca9706 cells were treated with a PI3K agonist in order to investigate the mechanism of action of psoralidin. It was observed that psoralidin was able to decrease the proliferation and promote the cellular apoptosis of Eca9706 cells in a dose-dependent manner. Furthermore, psoralidin was also able to inhibit the caspase-3 activity of Eca9706 cells in a dose-dependent manner. In addition, psoralidin inhibited NF-κB activity and reduced PI3K and Akt protein expression in Eca9706 cells. Notably, the PI3K agonist was able to reverse the effect of psoralidin on Eca9706 cells. The results of the present study demonstrated that psoralidin was able to inhibit proliferation and enhance apoptosis of human esophageal carcinoma cells via the NF-κB and PI3K/Akt signaling pathways.

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#26111475   2015/07/07 Save this To Up

Upregulation of Death Receptor 5 and Production of Reactive Oxygen Species Mediate Sensitization of PC-3 Prostate Cancer Cells to TRAIL Induced Apoptosis by Vitisin A.

Although Vitisin A, derived from wine grapes, is known to have cytotoxic, anti-adipogenic, anti-inflammatory and antioxidant effects, the underlying antitumor mechanism has not been investigated in prostate cancer cells to date. In the present study, the apoptotic mechanism of Vitisin A plus TNF-related apoptosis-inducing ligand (TRAIL) in prostate cancer cells was elucidated.

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Androgen Receptor (Phosph Androgen Receptor (Phosph Androgen Receptor (Ab 650 Opioid Receptor (Ab 375) AZD-3514 Mechanisms: Andr Dog Receptor-binding canc MarkerGeneTM Live Cell Fl Ofloxacin CAS Number [824 Estrogen Receptor á (Pho Estrogen Receptor á (Pho Estrogen Receptor á (Pho Estrogen Receptor á (Pho

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#25598954   2015/01/19 Save this To Up

Mir-55 inhibition can reduce cell proliferation and induce apoptosis in Jurkat (Acute T cell Leukemia) cell line.

MicroRNAs are small and non-coding RNA molecules with approximately 22 nt in length that cause inhibition of translation or degradation of mRNA. MiR-155 is a kind of molecule with different functions, such as its role in proliferation, apoptosis, inflammation, differentiation, and immunity. One of its best known functions is apoptosis that affects on caspase-3 activity. The main aim of this study was evaluation of miR-155 inhibition effect on cell proliferation and apoptosis induction in Jurkat cells.

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